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Cd11b-hCD89 Mouse
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Cd11b-hCD89 Mouse
Product Name
Cd11b-hCD89 Mouse
Product ID
C001793
Strain Name
C57BL/6NCya-Itgamem1(IRES-hFCAR)/Cya
Backgroud
C57BL/6NCya
Status
When using this mouse strain in a publication, please cite “Cd11b-hCD89 Mouse (Catalog C001793) were purchased from Cyagen.”
Product Type
Age
Genotype
Sex
Quantity
The standard delivery applies for a guaranteed minimum of three heterozygous carriers. Breeding services for homozygous carriers and/or specified sex are available.
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Basic Information
Validation Data
Related Resource
Basic Information
Gene Name
Itgam & FCAR
Gene Alias
CR3, CR3A, MAC1, Cd11b, Ly-40, Mac-1, Mac-1a, CD11b/CD18, F730045J24Rik, CD89, FcalphaR, FcalphaRI, CTB-61M7.2
NCBI ID
Chromosome
Chr 7 (Mouse), Chr 19 (Human)
MGI ID
--
Datasheet
Strain Description
CD89, also known as Fcα receptor (FCAR), is a receptor on the surface of various immune cells and belongs to the Fc receptor family. Fc receptors bind antibodies, linking the immune system’s recognition of pathogens with cellular immune responses. CD89 is primarily expressed on monocytes/macrophages, neutrophils, eosinophils, dendritic cells, and Kupffer cells in the liver, unlike other Fc receptors expressed on lymphocytes [1]. The function of CD89 primarily involves binding with IgA antibodies (especially IgA1 and IgA2), initiating various immune responses. CD89 can trigger phagocytosis (engulfing and destroying pathogens), antibody-dependent cellular cytotoxicity (ADCC) (killing infected or cancerous cells), and release inflammatory mediators (promoting inflammatory responses and recruiting immune cells) [2]. IgA nephropathy (IgAN) is a disease closely associated with CD89 and is the most common form of glomerulonephritis, characterized by the deposition of IgA (particularly IgA1) in the glomeruli. As the myeloid cell-specific Fc receptor for IgA, CD89 specifically binds IgA1, a highly glycosylated IgA subtype predominantly found in serum and responsible for neutralizing pathogens at mucosal surfaces [3-4]. In IgA nephropathy, one pathological mechanism is the formation of immune complexes between aberrantly glycosylated IgA1 and CD89. These complexes deposit in the glomerular mesangium, activate mesangial cells, and trigger inflammation, fibrosis, and kidney structural damage. Without treatment, the condition can progress to chronic kidney disease (CKD) and even end-stage renal disease (ESRD) [5-7].
Since mice lack a homologous gene to human CD89, introducing the human CD89 gene into mice aids in studying immune mechanisms and IgA nephropathy (IgAN). The Cd11b-hCD89 mice are a humanized model constructed by integrating the coding sequence (CDS) of the human CD89 gene downstream of the TAA stop codon of the mouse Cd11b (Itgam) gene. The human CD89 gene is specifically expressed in myeloid cells under the regulation of the mouse Cd11b gene promoter. Cd11b-hCD89 mice can be used in studies on immune responses, autoimmune mechanisms, as well as tumor and infectious diseases. They can also be crossed with the IgA1 humanized mouse model (Product No.: C001565) to construct an IgA nephropathy (IgAN) mouse model that better recapitulates human genetic mechanisms and pathological phenotypes [8], for researching IgAN mechanisms and developing therapies.
Reference
Monteiro RC, Van De Winkel JG. IgA Fc receptors. Annu Rev Immunol. 2003;21:177-204.
Ben Mkaddem S, Rossato E, Heming N, Monteiro RC. Anti-inflammatory role of the IgA Fc receptor (CD89): from autoimmunity to therapeutic perspectives. Autoimmun Rev. 2013 Apr;12(6):666-9.
Bakema JE, van Egmond M. The human immunoglobulin A Fc receptor FcαRI: a multifaceted regulator of mucosal immunity. Mucosal Immunol. 2011 Nov;4(6):612-24.
Robert T, Berthelot L, Cambier A, Rondeau E, Monteiro RC. Molecular Insights into the Pathogenesis of IgA Nephropathy. Trends Mol Med. 2015 Dec;21(12):762-775.
Stamellou E, Seikrit C, Tang SCW, Boor P, Tesař V, Floege J, Barratt J, Kramann R. IgA nephropathy. Nat Rev Dis Primers. 2023 Nov 30;9(1):67.
Suzuki H, Novak J. IgA Nephropathy: Significance of IgA1-Containing Immune Complexes in Clinical Settings. J Clin Med. 2024 Aug 1;13(15):4495.
Cheung CK, Alexander S, Reich HN, Selvaskandan H, Zhang H, Barratt J. The pathogenesis of IgA nephropathy and implications for treatment. Nat Rev Nephrol. 2024 Sep 4:10.
Papista C, Lechner S, Ben Mkaddem S, LeStang MB, Abbad L, Bex-Coudrat J, Pillebout E, Chemouny JM, Jablonski M, Flamant M, Daugas E, Vrtovsnik F, Yiangou M, Berthelot L, Monteiro RC. Gluten exacerbates IgA nephropathy in humanized mice through gliadin-CD89 interaction. Kidney Int. 2015 Aug;88(2):276-85.
Strain Strategy
The IRES-Kozak-Human FCAR CDS cassette was inserted downstream of the TAA stop codon.

Figure 1. Gene editing strategy of Cd11b-hCD89 mice.
Application Area
Research on immune responses and autoimmune mechanisms;
IgA nephropathy (IgAN) model establishment and drug efficacy evaluation;
Preclinical evaluation of CD89-targeted therapies;
Research on tumors and infectious diseases.
Validation Data
Related Resource
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